60 Advertorial
DELISENS™
: Providing relief to sensitive skin
A large percentage of the population suffers from sensitive skin, which is a disturbing skin condition that can detrimentally affect the quality of life. The most distinctive symptoms are prickling, burning, tingling, pain or itching, and occasionally, erythema and flush. Lipotec has developed DELISENS™ provide relief against these sensations
to
Sensitive skin is a skin disorder that can be induced by environmental factors (e.g. pollution, UV radiation, dryness, heat), lifestyle factors (e.g. cosmetics, soap), psychological factors (e.g. stress) or hormonal factors. Sensitive skin may worsen and give rise to inflammatory and/or pruritic chronic skin disorders such as Atopic Dermatitis (AD), dry skin and acne, which also share a common pattern of barrier impairment and increased vascular reactivity. Acute or chronic skin inflammation lowers the
threshold for pruritic stimuli which causes a peripheral itch sensitisation. Pruritus is induced by histamine in some itchy dermatoses; however, it is not the main pruritic mediator in the majority of diseases characterised by chronic itches such as atopic dermatitis. Proteases are more than just enzymes that
hydrolyse peptide bonds linking amino acids; they are a group of mediators that communicate with nerves, modulating inflammation, pain, and pruritus. Proteases from plants (e.g., pollen), mites (e.g., house dust mite), or human inflammatory cells (e.g.,
mast cell tryptase) can act as signalling molecules for pruritus and/or inflammation by cleaving the members of the family of G-protein coupled Proteinase-Activated Receptors (PARs), which play important roles in response to tissue injury, notably in the process of inflammation and repair. Proteinase-Activated Receptor 2 (PAR-2) is abundantly expressed by almost all cell types, especially by keratinocytes, but also in sensory neurons, and inflammatory cells. PAR-2 can be activated by trypsin-like serine proteases such as trypsin and tryptase during inflammation or hypersensitivity, mediating neurogenic inflammation and may trigger the sensation of pruritus and/or pain. Stimulation of PAR-2 on keratinocytes increases the secretion of inflammatory cytokines such as interleukin (IL)-6 and IL-8, mediating pruritus and/or inflammation in cases such as skin exposure to allergens, exogenous microbial proteases, or UV radiation. PAR-2 activation increases the excitability of neurons, and may sensitise their responses to
agonists of other receptors involved in inflammatory processes, such as the Transient Receptor Potential Vanilloid-1 (TRPV1) resulting in exacerbated inflammation and amplifying pain and itch sensation. The TRPV1 is a non-selective plasma-membrane cationic and heat-sensitive channel that mediates responses to a number of pain-inducing stimuli, including heat, protons, and chemical irritants, such as capsaicin, which causes burning pain or pruritus. TRPV1 is mainly expressed on sensory C-fibres by primary afferent nociceptive neurons and their terminals, so its activation can selectively sensitise these neurons and initiate neurogenic inflammation by releasing neuropeptides in the periphery, such as Calcitonin Gene-Related Peptide (CGRP) and Substance P (SP).
CGRP and SP act in a coordinated manner to cause cutaneous inflammation and oedema. CGRP stimulates arteriolar vasodilation and blood flow, and the combination of CGRP-induced hyperemia and SP-stimulated vascular permeability causes oedema. CGRP also potentiates the release of SP and inhibits
Placebo cream
Cream with 2% DELISENS™
SOLUTION
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